The Microbiologist sat quietly eating his lunch, partially hidden behind a pot plant in the staff canteen, when he sensed someone standing behind him. “Damn!” he thought, thinking he had hidden well enough to prevent his lunch being interrupted with any clinical questions... but clearly not.
 
Looking around he met the gaze of the Cardiology Registrar who was clearly waiting to make eye contact before launching into “the patient’s story”!
 
…“I have a patient in her early twenties who came in with a fever and a rash, but over the last few days she has started to go into heart failure”.
 
The Registrar had been in the Microbiologist’s teaching session early in the week, and had clearly “swotted up” after being asked questions he didn’t know the answers too.
 
The Cardiology Registrar then delivered the “piece de resistance” and declared “I think this might be Rheumatic Fever”.

“Okay, this is going to sound odd, but can we test a baby for RSV?” asked the Paediatrician.
 
“You do realise it’s July, don’t you? I mean I know we’ve all been locked in our houses for months, it’s raining and the radio played a Christmas song this morning…but it’s still summer!” exclaimed the Microbiologist.

“I have a patient in his 40s who has been coughing for several weeks and is starting to get fed up. The cough is keeping him, and his wife, awake, so he’s taken to sleeping in the spare room in order to give her some respite but it’s not ideal. I’ve done a chest x-ray and it looks okay, and he’s not really coughing anything up in order to send to it to the lab for culture. What antibiotics do you think I should give?” said the GP.

Malaria is a common parasitic infection spread by mosquitos. WHO estimate that there were 229 million cases occurring during 2019, with 409,000 deaths of which 274,000 were children under 5 years old. This is both staggering and depressing because malaria is both preventable and treatable… and yet every year over 400,000 people die who shouldn’t. That means more people have died in the last 8 years from malaria than have died in the Covid-19 pandemic.
 
Trillions of pounds have been spent during the Covid-19 pandemic supporting the economies of developed countries and yet only about 3 billion pounds has been spent in total trying to fight malaria. Why the difference? It could be that Covid-19 had the potential to cause more death and disease than malaria, but then why not spend the trillions on the health response rather than the economy? Could it have anything to do with the fact that 94% of cases and deaths from malaria occur in Africa rather than Europe and the USA?
 
Now we all know we should go and get our Covid-19 vaccine but wouldn’t it be great if there was an effective vaccine against malaria too? The WHO want a malaria vaccine that is at least 75% effective by the year 2030. Surely if there was something like that it would be all over the news; all that death and disease prevented. Well there is a promising vaccine… it just seems to have got a bit lost in all the Covid-19 noise… it is being trialled by those clever scientists from Oxford again, but it does have a rubbish name…!

The Microbiologist gave a big sigh. It was a beautiful spring day outside, perfect for hitting the forest trails, and here he was sat at the duty desk advising on how to treat athletes foot… he sighed again…
 
The phone rang and with a heavy heart the Microbiologist answered.
 
“I have a patient who I think has a fungal infection” said the voice on the other end of the line.
 
“Here we go again” thought the Microbiologist.
 
“What kind of fungal infection?”
 
“I’m not really sure. He has a lump on his foot which has been getting worse since he came back from Africa a few months ago” said the voice.
 
The Microbiologist sat up straight. This was more like it, something weird and wonderful.
 
“Who am I speaking to? What was your patient doing in Africa? Did he hurt himself, cuts to his feet, anything like that?”
 
“Oh sorry, it’s the Dermatologist here, busy clinic and forgot my manners. The patient was volunteering, helping to build a school in a rural village, he was there for a long time and I suspect as he was wearing flip-flops a lot, he had many scratches and cuts to his feet during that time. I thought it might be another case of sporotrichosis, but there is no sporotrichoid spread and the lump is completely painless. There does look to be a sinus forming as well. What do you think?”
 
“It does sound like eumycetoma. Here’s what I think we should do…”

The patient was in his 50s and had been previously fit and well, but had become unwell a few months earlier after working in his garden on a hot sunny day. After putting his shirt back on and coming inside his arm had started to itch. This had rapidly spread to his chest and then all over his body. It felt to the patient like he had insects crawling under and over his skin. Nothing helped. He bathed, got changed, took an antihistamine, all to no avail.
 
The following morning, after a terrible night’s sleep, the patient was covered in a scab like rash and the itching continued. He saw his GP who thought this was a probable contact dermatitis and gave advice accordingly.
 
Over the next couple of months things went from bad to worse. The itching continued, he couldn’t sleep, the rash and scabs spread, and he became convinced he was infested with bugs. In fact, the patient was able to squeeze “bug stuff” out of the scabs for his GP to see! The GP took skin samples and sent them off to the microbiology lab, but no parasites were seen and nothing infectious grew.

The patient was in her 20s and presented to her GP complaining of vague abdominal pain and weight loss. She had been “surfing the net” and was worried she might have caught Bilharzia when travelling in Africa as a student 6 years before. The Doctors mind flashed back to his own medical student elective in Malawi where he remembered being told something about Bilharzia affecting the bladder of those who, like him, went swimming in the shallows of the lake. He shuffled uncomfortably but tried to reassure her it was unlikely; she was adamant that she ought to be tested.
 
The Doctor phoned the duty Microbiologist to chat things through and the Microbiologist explained that “Bilharzia” not only affects the bladder but some species can cause intestinal infection too, so it was a possibility. They agreed that the Doctor would arrange for a number of stool samples to be sent to the microbiology laboratory as well as a blood test to look for infection. The Doctor wasn’t convinced but the patient was happy for the thoroughness of the investigation.

​What is Bilharzia?
Bilharzia is the common name for schistosomiasis, no not a new dog breed (clearly I’ve been watching too much of the BBC’s series “Pooch Perfect!”), but a parasitic infection caused by flukes that infect blood vessels. Bilharzia is named after Theodor Bilharz, a German doctor who first identified the parasitic cause way back in 1852 but who unfortunately later died, at the age of only 37, from complications of another waterborne-illness, typhoid, caught in Egypt!
 
There are five main species of Schistosome that infect humans in different areas of the World, although the first 3 are the more common:

• Schistosoma haematobium – Africa and the Middle East
• Schistosoma mansoni – Africa and South America
• Schistosoma japonicum – East Asia
• Schistosoma intercalatum – West and Central Africa
• Schistosoma mekongi – Cambodia and Laos

 
Schistosomiasis is more common in rural areas than in urban centres because the life cycle of the parasite requires fresh water snails and these are much less likely to be found in towns and cities. Risk of infection is higher in lakes, rivers and estuaries rather than open water as the snails live on grasses and reads at the banks of the water sources.
 
Schistosomiasis is endemic in many countries but few within these populations have a high enough burden of parasites to be symptomatic or turn into “patients”. In the UK most cases of schistosomiasis are associated with travel to endemic countries, especially Africa.
 
The life cycle of Schistosoma spp.
Each of the Schistosoma spp. has a specific snail species which they require for their life cycle to be completed:

• S. mansoni – Biomphalaria spp.
• S. haematobium and S. intercalatum – Bulinus spp.
• S. japonicum – Oncomelania spp.
• S. mekongi – Tricula spp.

 
The life cycle:
Parasite eggs are excreted into freshwater from the infected faeces of a human (or animal). These eggs hatch and the microscopic larvae penetrate into the freshwater snails where they undergo further maturation before being released back into the water 4-6 weeks later as infectious cercariae; they remain infectious for up to 2 days but they are more infectious when just released. The cercariae then penetrate through the skin, especially if it is waterlogged like “pruned feet in the bath”, of another unsuspecting human (or animal) where it migrates, via the bloodstream, to the liver. Here they mature into adults over the next 2-4 weeks. The adults then swim against the blood flow to reach the blood vessels supplying the intestines or bladder depending on the species of parasite. In the blood vessels male and female worms mate followed by the female producing eggs which penetrate out into the intestine or bladder and the cycle repeats itself. The adult female, is bigger than the male, at around 7-20 mm long… Yep that’s up to 2cm long… its huge… so yes, you would be able to see it without a microscope! Added to this horror, adult worms usually live for 5-7 years but have been known to survive for 30 years or more!

​How does schistosomiasis present?
S. haematobium primarily infects blood vessels supplying the bladder whereas the other Schistosoma spp. infect blood vessels supplying the bowel. Symptoms are therefore related to where the infection is happening in the body. Most infections are asymptomatic, especially in people from endemic countries who have developed immunity to the parasite and therefore do not get the hypersensitivity reactions which are characteristic of this infection.
 
The initial infection in schistosomiasis is known as “swimmer’s itch” because when the parasite penetrates through the swimmers skin it can cause a dermatitis reaction; this localised immune reaction only occurs with repeat exposure as it requires priming however you can still develop the later signs of infection without having had “swimmers itch”.
 
Katayama fever is the name given to the later acute hypersensitivity reaction to schistosomiasis occurring 3-8 weeks after the initial infection. It is caused by an immune response to the parasites within the blood stream. The symptoms of Katayama fever include sudden onset of fever, urticaria and angioedema, chills, myalgias, arthralgia, cough, diarrhoea, abdominal pain, and headache.
 
The most significant consequences of schistosomiasis are from chronic infections and are worse with high numbers of locally trapped eggs, longer duration of symptoms and a strong immune response:

• Intestinal – weight loss, iron deficiency anaemia, colonic ulceration, polyps and dysplasia (early cancer) and occasionally strictures and bowel obstruction
• Hepatosplenic – occlusion of portal veins causes portal hypertension and splenomegaly followed by the development of gastrointestinal varices and the possibility of variceal bleeding
• Pulmonary – occurs especially with hepatosplenic chronic infection where eggs bypass the liver to embolise the lungs causing pulmonary hypertension and cor pulmonale (heart failure due to pulmonary hypertension)
• Genitourinary – bladder fibrosis and calcification leading to urethral strictures, obstruction and renal failure as well as bladder cancer
• Neurological – worms can occasionally enter blood vessels to the spinal cord and brain causing nerve damage, cerebral lesions and encephalopathy

 
How is schistosomiasis diagnosed?
A clinical history suggesting possible exposure is the key to diagnosis in non-endemic countries like the UK. Patients with bladder schistosomiasis may have terminal haematuria (bleeding at the end of passing urine… this is not life-threatening bleeding as its name might suggest!)
 
The two main methods for diagnosing schistosomiasis are serology and microscopy.
 
Serology tests detect either antibodies or antigens. The antibody test is useful in returned travellers and becomes positive 6-12 weeks after infection however it doesn’t distinguish between past or current infection and so is of little use in patients from endemic countries. The antigen tests are of more use in that they detect active infection and can be additionally helpful as they become negative again 5-10 days after successful treatment. 
 
Microscopy can be performed on urine or stool depending on the species of interest. Each type of Schistosome spp. has a characteristic appearance, usually dependent on size, shape and the location of the operculum (the little pointy bit that sticks out from the egg and makes it look like a “speech bubble”).

​In the UK a combination of microscopy, antibody and antigen tests are recommended:

​Patients with schistosomiasis often also have a raised eosinophil count in peripheral blood and patchy shadowing on a chest x-ray - if they have respiratory symptoms. These should both resolve following correct treatment.
 
How is schistosomiasis treated?
The mainstay of treatment of schistosomiasis is the drug Praziquantel. Praziquantel works by damaging the surface of the worm as well as causing it to become paralysed. Praziquantel is not active against larvae so the infection has to have been present for at least 4-6 weeks before it will be effective. NB The damage to the surface of the worm can cause more antigens to leak out and worsen the hypersensitivity reaction so in acute infection it is essential to give steroids prior to Praziquantel to first dampen down this reaction.
 
Chronic schistosomiasis is treated with Praziquantel without steroids. The dose is dependent on the species:

​Patients should have follow up microscopy and antigen tests to look for cure as well as repeat blood eosinophil counts.
 
Attempts to prevent schistosomiasis are undertaken in endemic countries by trying to ensure clean water supplies, safe disposal of faeces and regular mass treatment of the population to reduce the amount of environmental contamination.
 
So our patient’s blood tests confirmed that she did indeed have active schistosomiasis and the laboratory where able to identify S. mansoni. She was treated with Praziquantel and her symptoms settled over the next few weeks. Her repeat tests all showed successful treatment and everyone was pleased; the patient was better, the Microbiologist had a good story for his next teaching session and the Doctor, although he had considered doing an antigen test on himself too, decided he’d just jot it down as a great case for his CPD portfolio… 

Okay so we’re all bored of Covid-19 right, but like-it-or-not it hasn’t gone away and whilst many think we are now in the second wave I would argue it’s still the first wave… it never disappeared, we just went into hiding and now we are “out” again nothing has really changed since the last big peak of cases. Or has it? Surely, we have learned something about this new disease this year… haven’t we?

Back in the blog in August called “My pandemic is worse than your pandemic” I mentioned I might do a future blog on the ancient disease called Cocoliztli, which I had never heard of before… well for once I’ve remembered I said I would do a particular topic and here it is!
 
So I’ve delve into my historical medical books (and Google!) to look further into the unknown pandemic of Cocoliztli.
 
It is well known that imported infections from Europe with the Spanish Conquistadors caused many deaths; Smallpox for example was imported in about 1520 and killed about 8 million people. In fact during the 16th Century about 90% of the native population of Mexico was wiped out by disease. But as if Smallpox wasn’t enough, this was followed in 1545 by the first Cocoliztli epidemic which killed a further 15 million people. Local people called this disease Cocoliztli or “pest” and as pandemics go this one seems pretty bad! A further Cocoliztli epidemic in 1576 killed another 50% of the population, so by this time more than 90% of the natives had been killed in just over 50 years!

“I have a patient with facial cellulitis but they’re not responding to antibiotics, my Consultant has asked me to find out if there is a stronger antibiotic we can give” said the oncall doctor.
 
The Microbiologist rolled his eyes; why do people persist in thinking about antibiotics in terms of “stronger” when what they really mean is “broader spectrum”!
 
“Why don’t you start by telling me something about the patient?” said the Microbiologist through gritted teeth.
 
“Oh, okay” said the Doctor, thinking this was just going to waste more of his precious time.
 
“She has just returned from trekking in Bolivia where they stayed in mud huts. The patient thinks they might have been bitten on the face as there were quite a lot of big beetles around. She now has a swollen right eye and we’ve been giving IV Teicoplanin but it hasn’t made any difference so we want to give her something… stronger.”
 
His curiosity piqued, the Microbiologist let the latest “stronger” slip past.
 
“Are both upper and lower eyelids swollen? What did the insects look like exactly?”